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为了研究缺氧性肺动脉高压形成的机理，采用核酸分子杂交技术观察缺氧对肺动脉内皮细胞（ＰＡＥＣ）血小板源性生长因子（ＰＤＧＦ）－Ａ链、－Ｂ链及其受体α、β亚基基因表达的影响。结果表明低氧和无氧（２．５％Ｏ２和０％Ｏ２）１．５、３ｈＰＡＥＣ的ＰＤＧＦ－Ａ链ｍＲＮＡ表达显著增加（Ｐ＜０．０１，ｖｓ常氧组），而６～４８ｈＰＤＧＦ－Ａ链ｍＲＮＡ表达水平无明显改变。低氧和无氧１．５～４８ｈ均能显著地增加ＰＡＥＣ的ＰＤＧＦ－Ｂ链ｍＲ－ＮＡ表达（Ｐ＜０．０５）。常氧条件下ＰＡＥＣ均能低水平地表达ＰＤＧＦ－α亚基受体和β亚基受体，低氧和无氧则上调此两受体ｍＲＮＡ表达水平（Ｐ＜０．０５）。由此说明缺氧不仅能使ＰＡＥＣ“旁分泌”ＰＤＧＦ参与肺动脉平滑肌细胞增殖调节，也使ＰＡＥＣ通过“自分泌”ＰＤＧＤ及上调其膜上的ＰＤＧＦ受体基因表达，参与缺氧肺动脉内皮细胞自身功能调节，从而在缺氧性肺动脉高压肺血管收缩反应增强及肺血管结构改建中发挥重要作用。
In order to study the mechanism of hypoxic pulmonary hypertension, the effect of hypoxia on proliferation of platelet-derived growth factor (PDGF) -A chain, B chain and its receptor α, β subunit of pulmonary artery endothelial cells (PAEC) Effects of gene expression. The results showed that the expression of PDGF-A mRNA in hypoxic and anaerobic (2.5% O2 and 0% O2) 1.5,3hPAEC groups increased significantly (P <0.01 vs. normoxia group), while PDGF- A chain mRNA expression levels did not change significantly. Hypoxia and anaerobic 1.5 ~ 48h can significantly increase PAEC PDGF-B chain mR-NA expression (P <0.05). Under normoxic condition, PAEC could express PDGF-α subunit receptor and β subunit receptor at low level, while both hypoxia and anaerobic increased mRNA expression of both receptors (P <0.05). Thus hypoxia can not only make PAEC “paracrine” PDGF involved in the regulation of pulmonary artery smooth muscle cell proliferation, but also to PAEC by “autocrine” PDGD and upregulation of PDGF receptor gene expression on its membrane involved in hypoxic pulmonary artery endothelial function Regulation, and thus hypoxic pulmonary hypertension pulmonary vasoconstriction reaction and pulmonary vascular remodeling play an important role.